The superoxide anion is involved in the induction of long-term potentiation in the rat somatosensory cortex in vitro.

The involvement of the superoxide anion (O2-) in the induction of neocortical long-term potentiation (LTP) was examined in rat brain slices containing the primary somatosensory cortex. Field potentials evoked by stimulation in cortical layer IV were recorded from layer II/III. In control experiments, tetanic high-frequency stimulation (HFS) resulted in essentially input-specific, NMDA receptor-dependent LTP (20.2+/-3.0% increase in field potential amplitude). When the availability of intracellular O2- was reduced by application of the cell membrane-permeable O2- scavengers MnTBAP or CP-H (spin trap), HFS-induced LTP was attenuated to 12.0+/-1.7% and 8.7+/-3.1% increase, respectively. In contrast, HFS-induced LTP was not significantly affected by the cell membrane-impermeable O2- scavenger superoxide dismutase (SOD). Induction of the generation of O2- by the cell membrane-permeable redox-cycling quinone DMNQ resulted in a HFS-independent slow-onset LTP (21.8+/-6.0%) in three of eight brain slices. Together, these results suggest the contribution of O2- to the induction of LTP in the primary somatosensory cortex by an action on intracellular induction mechanisms.